Professional Documents
Culture Documents
ScienceDirect
journal homepage: www.elsevier.com/locate/psyneuen
Received 26 November 2014; received in revised form 10 February 2015; accepted 27 February 2015
KEYWORDS
Testosterone;
Cortisol;
Risk-taking;
Impulsivity;
Traits
Summary Recent theories propose that testosterone should be positively related to risktaking, but empirical support is mixed. Building on the dual-hormone hypothesis, the present
research tested whether testosterones role in risk-taking depends on cortisol. Study 1 (N = 115)
tested this hypothesis in a mixed-sex sample with self and informant reports of risk-taking. Study
2 (N = 165) tested this hypothesis in a male-only sample with the Balloon Analog Risk Task, a
behavioral measure of risk-taking. Across both studies, there was a positive association between
basal testosterone and risk-taking among individuals low in basal cortisol but not individuals high
in basal cortisol. This pattern emerged in both males and females and across multiple measures
of risk-taking (self reports, informant reports, behavior). These studies provide novel empirical
support for the claim that testosterone and cortisol jointly regulate risk-taking. Discussion
focuses on putative mechanisms as well as implications for real-world risk-taking behaviors.
2015 Elsevier Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.psyneuen.2015.02.023
0306-4530/ 2015 Elsevier Ltd. All rights reserved.
1. Study 1
Study 1 tested whether the interaction between basal
testosterone and basal cortisol predicted trait risk-taking,
which was assessed through a self-report scale (Zuckerman,
89
1991) as well as judgments by informantswell-acquainted
individuals such as friends, signicant others, and family
members (Funder and Colvin, 1988; Vazire, 2006, 2010;
Vazire and Carlson, 2011). Although self-reports are reasonably accurate predictors of behavior, they are susceptible
to cognitive and motivational biases (e.g., the motivation
to present oneself in a desirable manner). Informant ratings
are advantageous because they predict behavior above and
beyond self-reports (Vazire, 2010; Vazire and Carlson, 2011).
A combination of self and informant reports provide a more
complete picture of a persons behavioral tendencies than
either perspective alone. Moreover, a dual-hormone interaction on self-reported risk-taking is more likely to be driven
by a common third variable compared to a dual-hormone
interaction on informant-reported risk-taking. Hence, the
use of informant reports likely provides a more stringent
test of the dual-hormone hypothesis. We conducted analyses
to test whether testosterone and cortisol jointly predicted
self- and informant-reported trait risk-taking.
1.1. Methods
1.1.1. Participants
Participants (N = 115) between the ages of 18 and 30 years
were recruited to control for age-related changes in steroid
hormones and risk-taking (46.1% male, mean age: 20.57;
SD = 2.82). Participants were a mix of students and community participants in the greater Austin area who completed
the study in exchange for payment. Compensation varied
between $10 and $25 depending on decisions made in tasks
unrelated to the current research questions. The sample
was diverse (48.2% Caucasian, 7.1% African-American, 27.7%
Asian, 14.3% Latino, 2.7% who reported mixed ethnicity).
By the standards of Cohen (1988, 1992), this sample size
has adequate power (power > .80) to detect effects of a
magnitude of Pearsons r = .26 and above. All procedures
received ethics approval from the UT-Austin Institutional
Review Board.
1.1.2. Materials and procedure
1.1.2.1. Self-reported trait risk-taking. Participants completed online self-report measures prior to reporting to
the lab. Self-reported trait risk-taking was assessed using
Zuckermans impulsive sensation-seeking scale (1991). This
scale consists of nineteen true or false items concerning
the tendency to take risks for the purpose of excitement
and having unique experiences ( = .83). Scores on this
scale have been shown to predict risk-taking behaviors
(e.g., Hoyle et al., 2000; Zuckerman and Kuhlman, 2000;
Steinberg, 2008; Pharo et al., 2011; Lauriola et al., 2014).
1.1.2.2. Saliva samples and informant contact information.
After completing the online measures, participants reported
to the lab between 1030 h and 1730 h. Participants provided
informed consent, lled out questionnaires relevant to hormone measurement, and then provided a 2 mL saliva sample
(Schultheiss and Stanton, 2009). The sample was immediately transported to a freezer. Participants were also asked
to nominate at least one person to provide information on
their personality (Vazire, 2006). Participants provided email
addresses for one to three informants and were told that
these informants would be contacted to ll out a short
90
survey as part of the study. Participants then completed
tasks that were unrelated to research questions in the current paper and were paid for their participation.
1.1.2.3. Informant-reported risk-taking. We followed
published guidelines for collecting informant report data
(Vazire, 2006). Informants were contacted via email using
standardized text. The email indicated that [Name of
participant] (referred subsequently to as X) recently
participated in a psychology study and nominated them
to provide information about Xs personality. Informants
were then given a unique id number and were directed
to a website that included a personality questionnaire
about X. Informants lled out an online consent form
prior to lling out the questionnaire. Informants were
told that their responses would be used for psychological
research only and would not be shared. No compensation
was given to informants. If informants did not complete
the questionnaire after the rst email, a second reminder
email was sent. Comparable to previous research, at least
one informant provided ratings for 81% of the sample
(Vazire, 2006). Among those participants with at least one
informant rating, the average number of informants was
1.84 (SD = 0.73; approximately 35% had ratings from one
informant, 45% had ratings from two informants, and 20%
had ratings from three informants).
The informant report questionnaire included two facevalid items that assessed risk-taking. Informants were asked
to indicate to what extent they saw X as someone who
enjoys taking risks and tends to play it safe using
a 7-point Likert type scale (1 = Disagree Strongly, 7 = Agree
Strongly). We reverse coded the second item. Ratings on
these items were highly correlated (r = .54, p < .001, Cronbachs = .70) and thus were averaged to form one index
of informant-reported risk-taking. For those participants for
whom multiple informants completed the questionnaire, we
averaged across informant ratings.
1.1.2.4. Hormone assays. Saliva samples were stored in
polystyerene tubes and frozen at 20 C. Once data collection was complete, the samples were shipped frozen
overnight to Yerkes Endocrine Core Laboratory (Emory University, Atlanta, GA) and were assayed for testosterone and
cortisol using radioimmunoassay kits purchased from Diagnostic Systems Laboratories, Inc. Intra-assay variability for
testosterone averaged 8%, and inter-assay variability averaged 11%. Intra-assay variability for cortisol averaged 6%,
and inter-assay variability averaged 10%.
1.2. Results
1.2.1. Preliminary analyses
Tables 1 and 2 display zero-order correlations and descriptive statistics for the entire sample (Table 1), as well
as for males and females separately (Table 2). As noted
in the tables, there is a moderate correlation between
self-reports and informant reports of trait risk-taking.
The size of the correlation is consistent with selfinformant agreement for other traits (Vazire, 2006). As
expected, an independent samples t-test (equal variances not assumed) revealed that mens testosterone
levels (M = 141.90, SD = 39.53) were higher than womens
(M = 27.27, SD = 11.32), t(59.42) = 20.40, p < .001, d = 5.30,
95% CI: 103.39, 125.88).1 However, men and women did
not differ in basal cortisol (t(110) = .93, p = .355, d = .18),
self-reported risk taking (t(113) = .36, p = .723, d = .07),
or informant-reported risk-taking (t(92) = .49, p = .624,
d = .10). This non-signicant sex difference in risk-taking
measures converges with recent meta-analyses, which found
only small aggregate effect sizes for sex differences in
risk-taking (Lauriola et al., 2014; Nelson, 2014). These metaanalyses included several individual studies that also found
non-signicant sex differences in risk-taking in line with
the present results. Consistent with previous research (e.g.,
Popma et al., 2007; Mehta et al., 2008; Mehta and Josephs,
2010), testosterone and cortisol (log10 transformed) were
moderately correlated (r = .38, p < .001). Although time of
day was associated with testosterone (standardized within
sex, r = .24, p = .009) and cortisol (r = .40, p < .001), age
was not associated with testosterone (r = .03, p = .795) and
marginally associated with cortisol (r = .17, p = .066).
1.2.2. Testosterone, cortisol, and trait risk-taking
Moderated regression analyses were used to examine
whether testosterone and cortisol interacted to predict risk
taking. These analyses were conducted in two separate
regression models for self-reported and informant-reported
risk taking. The results of these analyses are displayed in
Table 3.
1.2.2.1. Self-reported trait risk-taking. Consistent with
the dual-hormone hypothesis, there was a statistically signicant testosterone cortisol interaction for self-reported
trait risk-taking ( = .22, CI95 : [6.06, .52], rpartial = .22
p = .020). Simple slopes analyses (Aiken and West, 1991)
revealed that testosterone was positively associated with
self-reported risk-taking when cortisol was low (b = 1.78,
se = .64, t(106) = 2.79, p = .006). However, when cortisol was
high (+1 SD), the association between testosterone and selfreported risk-taking was non-signicant (b = .10, se = .54,
1.
2.
3.
4.
5.
6.
7.
8.
91
T (pg/mL)
C (ng/mL)
ZT
Clog10
Self-report RT
Inf. report RT
Age
Time
SD
80.56
.21
.01
.77
9.46
4.20
20.53
14:44
63.91
.17
1.00
.28
4.43
1.22
2.82
2:36
114
112
112
112
115
94
115
115
.19*
.38***
.20*
.01
.07
.18
.14
.24*
.90***
.04
.20
.20*
.34***
.29**
.16
.03
.03
.24**
.07
.11
.17
.40***
.43***
.04
.01
.16
.08
.20*
p < .07.
p < .05.
** p < .01.
*** p < .001.
Note: T = testosterone, C = cortisol, ZT = testosterone standardized within sexes, Clog10 = log transformed cortisol, Self-report RT = selfreported trait risk-taking, Inf. report RT = informant-reported trait risk-taking, Time = time of saliva sample.
*
Table 2
Correlations and descriptive statistics for Study 1 (males and females separated).
Men
1.
2.
3.
4.
5.
6.
7.
T (pg/mL)
C (ng/mL)
Clog10
Self-report RT
Inf. report RT
Age
Time
.31*
.29*
.10
.14
.03
.34*
Women
1.
2.
3.
4.
5.
6.
7.
T (pg/mL)
C (ng/mL)
Clog10
Self-report RT
Inf. report RT
Age
Time
.17
.29*
.20
.14
.11
.16
SD
.17
141.90
.23
.74
9.30
4.13
21.15
14:38
39.53
.19
.28
4.28
1.09
3.29
2:40
53
51
51
53
43
53
53
SD
27.27
.20
.79
9.60
4.26
20.00
14:50
11.32
.15
.283
4.58
1.33
2.23
2:33
61
61
61
62
51
62
62
.89***
.19
.21
.28*
.28*
2
.28*
.12
.24
.32*
3
.30*
.15
.01
4
.27
.20
5
.92***
.11
.19
.03
.40**
.09
.09
.06
.47***
.52***
.11
.04
.08
.02
.24
p < .07.
p < .05.
** p < .01.
*** p < .001.
Note: T = testosterone, C = cortisol, ZT = testosterone standardized within sexes, Clog10 = log transformed cortisol, Self-report RT = selfreported trait risk-taking, Inf. report RT = informant-reported trait risk-taking, Time = time of saliva sample.
*
92
Table 3 Multiple regression model of testosterone cortisol interaction predicting self-reported and informant reported risktaking (n = 110 for self reports, n = 92 for informant reports).
t(106)
rpartial
95% CI
.84
.15
3.29
.19
.01
.22
1.93
.10
2.36
.056
.922
.020
.18
.01
.22
(.02, 1.70)
(2.88, 3.18)
(6.06, .52)
t(88)
rpartial
95% CI
.18
.66
1.18
.15
.16
.31
1.38
1.52
3.02
.170
.133
.003
.15
.16
.31
(.08, .43)
(1.52, .21)
(1.96, .40)
Notes.
B indicates unstandardized regression coefcients. indicates standardized regression coefcients.
a Log-transformed because of skew in the distribution.
b Interaction term computed from mean centered predictors.
2. Study 2
Study 1 demonstrated that endogenous cortisol and testosterone interact to predict risk-taking in line with the
dual-hormone hypothesis. The results conceptually replicated with self and informant reports of trait risk-taking.
An important next step is to test whether this dual-hormone
interaction extends to a behavioral measure of risk-taking
in an independent sample. Study 2 was designed to test the
synergistic effects of endogenous testosterone and cortisol
on a validated laboratory task of risk-taking behavior: the
Balloon Analog Risk Task (BART) (Lejuez et al., 2002). We
used a well-powered sample of men who provided saliva
samples and completed the BART. Based on the predictions
of the dual-hormone hypothesis, we expected that testosterone and cortisol would interact to predict risk-taking
behavior such that testosterone would be positively related
to risk-taking only among low-cortisol individuals but not
among high-cortisol individuals.
2.1. Methods
2.1.1. Participants
Participants were 165 male undergraduate students
(Mage = 20.64, SD = 3.00) from Wayne State University who
participated for partial course credit. The sample was
diverse (38.2% Caucasian, 19.4% Black, 18.1% Asian, 4.8%
Latino, .6% Native American, and 18.8% Other). This study
was part of a larger research protocol examining the
role of hormones and individual differences predicting
risk taking (e.g., Welker et al., in press). The results
presented here do not overlap with previously published
research. Two participants were missing cortisol data,
two were missing both cortisol and testosterone data,
and one participant failed to understand the directions on the risk taking measure. Thus, the nal sample
size consisted of 160 participants, which had adequate
power (.8) to detect effects greater than or equal to
r = .22.
93
Figure 1 Self-reported and informant-reported risk taking as a function of testosterone and cortisol (Study 1). Note: Plotted points
represent conditional low and high values (1 SDs) of testosterone (standardized within each sex) and cortisol (log-transformed)
2.2. Results
2.2.1. Preliminary analyses
Table 4 presents the descriptive statistics and correlations
for the measures included in Study 2. Consistent with Study
1, testosterone and cortisol (log10 transformed) were moderately correlated (r = .33, p < .001). Time of day was not
signicantly associated with testosterone (r = .07, p = .389)
or transformed cortisol concentrations (r = .04, p = .635).
Age was unrelated to testosterone levels (r = .08, p = .299),
but had a marginally signicant, negative association with
transformed cortisol (r = .16, p = .051).
2.2.2. Testosterone, cortisol, and risk-taking behavior
Moderated regression analyses were used to assess whether
testosterone and cortisol interacted to predict risk-taking
behavior. Testosterone and transformed cortisol concentrations were mean-centered and multiplied to create
an interaction term. The results of this analysis are
presented in Table 5. Conceptually replicating Study 1,
there was a statistically signicant testosterone cortisol
94
Table 4
1.
2.
3.
4.
5.
6.
*
**
T (pg/mL)
C (ng/mL)
Clog10
Risk taking
Age
Time of day
SD
102.48
2.97
0.33
9.81
20.64
13.17
40.65
3.55
0.34
3.21
3.00
1.46
163
161
161
164
163
165
.19*
.33**
.01
.08
.07
.77**
.04
.12
.04
.07
.16
.04
.09
.01
.00
p < .052.
p < .02.
p < .001.
Table 5
Multiple regression model of testosterone cortisol interaction predicting risk-taking behavior (n = 160 men).
t(156)
rpartial
95% CI
.00
.48
.05
.06
.05
.22
.65
.62
2.67
.516
.537
.008
.05
.05
.21
(.01, .02)
(1.06, 2.03)
(.08, .01)
Notes.
B indicates unstandardized regression coefcients. indicates standardized regression coefcients.
a Log-transformed because of skew in the distribution.
b Interaction term computed from mean centered predictors.
to this model did not alter the signicance of the testosterone cortisol interaction ( = .21, CI95 : [.08, .01],
rpartial = .21, p = .011).6
3. Discussion
Previous studies have demonstrated that testosterone
interacts with cortisol to predict behaviors related to
dominance, aggression, and social status (Dabbs et al.,
1991; Popma et al., 2007; Mehta and Josephs, 2010; Geniole
et al., 2011; Denson et al., 2013; Edwards and Casto, 2013;
Pfattheicher et al., 2013; van Den Bos et al., 2013; Tackett
et al., 2014; Welker et al., 2014; Zilioli et al., 2014b). The
present research provides new evidence that testosterone
and cortisol interact to predict risk-taking. Across two
studies (total N = 280), we found a positive association
between basal testosterone and risk-taking among low
basal cortisolbut not high basal cortisolindividuals. This
effect was evident in both males and females and replicated across measures of self-reported trait risk-taking,
informant-reported trait risk-taking, and risk-taking behavior. The fact that the results emerged on three different
markers of risk-taking in two independent samples provides
greater condence in the robustness of the effects. These
ndings advance knowledge on the neuroendocrinology
of risk-taking in suggesting that testosterone and cortisol
work in concert to regulate risk-taking according to the
predictions of the dual-hormone hypothesis (Mehta and
Josephs, 2010) (for a related theory that predicts hormone
ratio effects instead of statistical interaction effects, see
Terburg et al., 2009; Montoya et al., 2012).
A viable mechanism for the current results resides in
the functional crosstalk between the HPG and HPA axis,
with cortisol potentially buffering the pathway between
testosterone and risky behavior. Glucocorticoids inhibit HPG
axis function at multiple levels, decrease androgen receptor levels, and suppress the effects of testosterone on
target tissues (Smith et al., 1985; Johnson et al., 1992;
Burnstein et al., 1995; Chen et al., 1997; Tilbrook et al.,
2000; Viau, 2002; Lin et al., 2014), which all may lead to
an inhibitory effect of elevated cortisol on testosterones
behavioral effects. Specically, when HPA axis activity is
reduced as reected by low cortisol levels, the reproductive axis may operate efciently leading to a robust positive
effect of testosterone on risk-taking. In contrast, when HPA
axis activity is heightened (i.e. high cortisol), the reproductive axis may be blocked or inhibited resulting in a null
association between testosterone and risk-taking.
A related mechanism for dual-hormone effects on risktaking is through increased activity in neural systems
implicated in reward sensitivity. In both animal and human
studies, testosterone boosts reward-seeking behaviors, psychological states associated with reward (e.g., enjoyment,
Mehta et al., 2014), and anticipation of reward via interactions with dopamine in the ventral striatum (e.g., nucleus
accumbens) (Packard et al., 1997, 1998; Van Honk et al.,
2004; Hermans et al., 2010; Op de Macks et al., 2011).
In contrast, exogenous cortisol down-regulates activity in
a neural reward network including the ventral striatum
(Montoya et al., 2014; but see also Lewis et al., 2014), and
activity in this region predicts increased risk-taking behaviors (Galvan et al., 2007; Rao et al., 2008; Somerville et al.,
2010). Thus, the joint effect of testosterone and cortisol
on risk-taking may be driven by the reinforcing effects of
dopamine in these motivational and reward regions of the
mesolimbic pathway.
95
A third putative mechanism for dual-hormone interactions on risk-taking may be through inhibition of pre-frontal
regions implicated in self-regulation and impulse control
(e.g., orbitofrontal cortex, OFC). Reduced OFC activity is
related to risky decisions (Eshel et al., 2007), and testosterones association with increased risk-taking and impulsive
aggression is explained by reduced OFC engagement (Mehta
and Beer, 2010) as well as reduced OFC volume (in males,
Peper et al., 2013). In contrast, heightened cortisol during risk-taking is associated with increased OFC activity
(Freeman and Beer, 2010). Further, testosterone reduces
functional connectivity between the OFC and subcortical
regions such as the amygdala (van Wingen et al., 2010;
Spielberg et al., 2014), and cortisol is related to increased
functional connectivity between the medial prefrontal cortex and amygdala (Veer et al., 2012). These ndings
suggest that dual-hormone interactions on risk-taking may
be explained by structural and functional differences in the
OFC as well as prefrontalsubcortical connectivity.
The current ndings may also reect hormonal interactions between approach and avoidance motivational systems
(Carver and White, 1994). Testosterone has been associated
with approach-oriented (e.g., dominance motivation, Mazur
and Booth, 1998) and appetitive motivation (e.g., Packard
et al., 1997; Van Honk et al., 2004; Hermans et al., 2010; Op
de Macks et al., 2011), whereas cortisol is associated with
social evaluative stress and behavioral inhibition (Dickerson
and Kemeny, 2004; Roelofs et al., 2009). Thus, a prole of
high testosterone (approach and appetitive motivation) and
low cortisol (low behavioral inhibition) may lead to heightened risk-taking, whereas the greater behavioral inhibition
tendencies associated with high cortisol may counteract the
inuence of high testosterone on risk-taking behavior (for
similar arguments, see Popma et al., 2007; Terburg et al.,
2009; Mehta and Josephs, 2010; Carr and Mehta, 2011;
Maner et al., 2012; Montoya et al., 2012).
The present results have implications for risky behaviors
in a number of different domains. The trait and behavioral risk-taking measures examined in the present studies
are reliable predictors of real-world risk-taking behaviors,
including sexual risk-taking, substance use, and dangerous
driving (Hoyle et al., 2000; Zuckerman and Kuhlman, 2000;
Lejuez et al., 2002, 2003; Hunt et al., 2005; Steinberg,
2008; Pharo et al., 2011; Lauriola et al., 2014;). Thus,
an important extension of the current research will be to
investigate whether testosterone and cortisol interact to
predict these real-world risk-taking behaviors as well (see
also Tackett et al., 2014). Another future direction will be
to test the dual-hormone hypothesis on nancial risk preferences. Indeed, overly risky nancial decisions can lead
to devastating monetary losses for the self and others, and
stable and uctuating components of the endocrine system
are theorized to play a role in the macro-level behavior of
nancial markets (Coates and Herbert, 2008; Apicella et al.,
2014; Kandasamy et al., 2014).
The current research may also inform developmental
theories of risk-taking. Risk-taking is heightened during
adolescence (Figner et al., 2009), and one of the leading
causes of death among this age group can be attributed
to poor and risky choices (e.g., motor-vehicle crashes,
other unintentional injuries; Eaton et al., 2008). Developmental researchers have theorized that pubertal increases
96
in sex hormones such as testosterone may increase risky
behavior (Somerville et al., 2010; Peper et al., 2013), but
the present study brings up the possibility that pubertal testosterone may interact with cortisol to modulate
risky decision-making in adolescents (see related evidence
for dual-hormone interactions predicting externalizing psychopathology in adolescents, Tackett et al., 2014). Further,
changes in risky decisions have been observed in older
adults compared to younger adults (Mata et al., 2011). Thus,
we suspect that the dual-hormone hypothesis may potentially explain changes in risk-taking throughout the lifespan
including older adulthood.
The present ndings also have implications for biosocial
theories of status attainment. Status in face-to-face groups
can be dened as an individuals prominence, respect, and
inuence in the eyes of others (Anderson and Kilduff, 2009).
Males in particular take risks in order to out-compete rival
males for the attention of attractive females, and these
risk-taking behaviors may increase access to mating opportunities and enhance ones status (Daly and Wilson, 1997;
Ronay and von Hippel, 2010; Ellis et al., 2012). In support
of a relationship between risk-taking and status pursuit,
research indicates that the presence of peers increases
risk-taking compared to the absence of peers among adolescents through enhanced reward processing (ventral striatum
activity; Chein et al., 2011). These results suggest that
heightened risk-taking may be a behavioral strategy aimed
at enhancing ones reputation in the eyes of others especially during adolescence (Ellis et al., 2012). However, it
remains unclear to what extent risk-taking in the present
research was inuenced by status concerns. Future research
should build upon the present ndings by considering contextual factors such as the presence versus absence of peers
in order to understand how dual-hormone interactions are
related to risk-taking in the pursuit of social status.
There are several limitations of the present research that
should be addressed in future studies. First, we assessed late
morning or afternoon hormone concentrations and examined their associations with risk-taking. Testosterone and
cortisol measured around the same time of day are moderately stable across several weeks (Liening et al., 2010),
suggesting they are reasonable measures of basal testosterone and cortisol. Test-retest reliability of these two
hormones along with evidence for testretest reliability
of the risk-taking measures we employed (Zuckerman and
Kuhlman, 2000; White et al., 2008) suggest that the current results are likely driven by associations between stable
hormone proles and stable risk-taking propensity. Nevertheless, there are diurnal rhythms in testosterone and
cortisol, and these hormones can uctuate in decisionmaking contexts (e.g., Coates and Herbert, 2008; Apicella
et al., 2014). Thus, it will be important for future studies
to collect additional saliva samples in order to investigate
stable and uctuating components of the HPG and HPA axes.
Second, we cannot be certain that testosterone and cortisol
have causal inuences on risk-taking because we measured
endogenous hormone concentrations. Future studies that
pharmacologically manipulate testosterone and cortisol are
needed to conrm causality. Third, although we tested the
dual-hormone hypotheses on widely used trait and behavioral measures of risk-taking, it is important to extend the
results of the present study to other behavioral measures of
Conict of interest
The authors declare no conicts of interest.
Acknowledgments
We thank Lisa Benavides, David Frederick, Celina Gonzalez, Robert Josephs, Adam Massman, Elyse McCutcheon,
Will McKinnon, Ryan Norcross, Shannon Parker, Linda Pham,
Daniel Pickhardt, Puya Rezee, Rishi Sawhney, Kelsey Schults,
Sasha Simon for data collection assistance in Study 1; Elianna
Lozoya, Brian Tyminski, Jordan Liphardt, Shyneth Galicia,
Nicholas Jones, and Dylan Sedam for data collection assistance in Study 2; and Cassandra Brandes for logistical
assistance in preparing the manuscript for publication.
References
Aiken, L.S., West, S.G., 1991. Multiple Regression: Testing and Interpreting Interactions. Sage.
Anderson, C., Kilduff, J., 2009. The pursuit of status in social groups.
Curr. Dir. Psychol. Sci. 18, 295298.
Apicella, C.L., Dreber, A., Campbell, B., Gray, P.B., Hoffman, M.,
Little, A.C., 2008. Testosterone and nancial risk preferences.
Evol. Hum. Behav. 29 (6), 384390.
Apicella, C.L., Dreber, A., Mollerstrom, J., 2014. Salivary testosterone change following monetary wins and losses predicts
future nancial risk-taking. Psychoneuroendocrinology 39,
5864.
Bechara, A., Damasio, A.R., Damasio, H., Anderson, S.W., 1994.
Insensitivity to future consequences following damage to human
prefrontal cortex. Cognition 50 (1), 715.
Blair, C., Peters, R., Granger, D., 2004. Physiological and neuropsychological correlates of approach/withdrawal tendencies
in preschool: further examination of the behavioral inhibition
system/behavioral activation system scales for young children.
Dev. Psychobio. 45, 113124.
Boksem, M.A., Mehta, P.H., Van den Bergh, B., van Son, V.,
Trautmann, S.T., Roelofs, K., Smidts, A., Sanfey, A.G., 2013.
Testosterone inhibits trust but promotes reciprocity. Psychol.
Sci. 24 (11), 23062314.
Burnstein, K., Maiorino, C., Dai, J., Cameron, D., 1995. Androgen and glucocorticoid regulation of androgen receptor cDNA
expression. Mol. Cell. Endocrinol. 115, 177186.
Campbell, B.C., Dreber, A., Apicella, C.L., Eisenberg, D.T., Gray,
P.B., Little, A.C., Garcia, J.R., Zamore, R.S., Lum, J.K., 2010.
Testosterone exposure, dopaminergic reward, and sensationseeking in young men. Physiol. Behav. 99 (4), 451456.
Carr, J.M., Mehta, P.H., 2011. Importance of considering
testosteronecortisol interactions in predicting human aggression and dominance. Aggress. Behav. 37, 13.
Caruthers, A.S., Van Ryzin, M.J., Dishion, T.J., 2014. Preventing
high-risk sexual behavior in early adulthood with family interventions in adolescence: outcomes and developmental processes.
Prev. Sci. 15 (1), 5969.
Carver, C.S., White, T.L., 1994. Behavioral inhibition, behavioral
activation, and affective responses to impending reward and
punishment: the BIS/BAS Scales. J. Pers. Soc. Psychol. 67,
319333.
Castellanos-Ryan, N., Parent, S., Vitaro, F., Tremblay, R.E., Sguin,
J.R., 2013. Pubertal development, personality, and substance
use: a 10-year longitudinal study from childhood to adolescence.
J. Abnorm. Psychol. 122 (3), 782.
Chein, J., Albert, D., OBrien, L., Uckert, K., Steinberg, L., 2011.
Peers increase adolescent risk taking by enhancing activity in
the brains reward circuitry. Dev. Sci. 14 (2), F1F10.
Chen, S., Wang, J., Yu, G., Liu, W., Pearce, D., 1997. Androgen
and glucocorticoid receptor heterodimer formation. A possible
mechanism for mutual inhibition of transcriptional activity. J.
Biol. Chem. 272, 1408714092.
Coates, J.M., Herbert, J., 2008. Endogenous steroids and nancial
risk taking on a London trading oor. Proc. Natl. Acad. Sci. U. S.
A. 105 (16), 61676172.
Cohen, J., 1988. Statistical Power Analysis for the Behavioral Sciences, 2nd ed. Lawrence Earlbaum Associates, Hillsdale, NJ.
Cohen, J., 1992. Statistical power analysis. Curr. Dir. Psychol. Sci.
1 (3), 98101.
Cumming, G., 2013. The new statistics: why and how. Psychol. Sci.
25 (1), 729.
Dabbs Jr., J.M., Jurkovic, G.J., Frady, R.L., 1991. Salivary testosterone and cortisol among late adolescent male offenders. J.
Abnorm. Child Psychol. 19 (4), 469478.
97
Daly, M., Wilson, M., 1997. Crime and conict: homicide in evolutionary psychological perspective. Crime Just., 51100.
Denson, T.F., Mehta, P.H., Ho Tan, D., 2013. Endogenous testosterone and cortisol jointly inuence reactive aggression in
women. Psychoneuroendocrinology 38 (3), 416424.
Derntl, B., Pintzinger, N., Kryspin-Exner, I., Schpf, V., 2014. The
impact of sex hormone concentrations on decision-making in
females and males. Neuroendocr. Sci. 8, 352.
Dickerson, S.S., Kemeny, M.E., 2004. Acute stressors and cortisol
responses: a theoretical integration and synthesis of laboratory
research. Psychol. Bull. 130 (3), 355.
Eaton, D.K., Kann, L., Kinchen, S., Shanklin, S., Ross, J., Hawkins,
J., Centers for Disease Control and Prevention (CDC), 2008.
Youth risk behavior surveillanceUnited States, 2007. MMWR
Surveill. Summ. 57 (4), 1131.
Edwards, D.A., Casto, K.V., 2013. Womens intercollegiate athletic competition: cortisol, testosterone, and the dual-hormone
hypothesis as it relates to status among teammates. Horm.
Behav. 64 (1), 153160.
Ellis, B.J., Del Giudice, M., Dishion, T.J., Figueredo, A.J., Gray, P.,
Griskevicius, V., Wilson, D.S., 2012. The evolutionary basis of
risky adolescent behavior: implications for science, policy, and
practice. Dev. Psychol. 48 (3), 598.
Eshel, N., Nelson, E.E., Blair, R.J., Pine, D.S., Ernst, M., 2007.
Neural substrates of choice selection in adults and adolescents:
development of the ventrolateral prefrontal and anterior cingulate cortices. Neuropsychologia 45 (6), 12701279.
Evans, K.L., Hampson, E., 2014. Does risk-taking mediate the relationship between testosterone and decision-making on the Iowa
Gambling Task? Pers. Individ. Diff. 61, 5762.
Figner, B., Mackinlay, R.J., Wilkening, F., Weber, E.U., 2009. Affective and deliberative processes in risky choice: age differences
in risk taking in the Columbia Card Task. J. Exp. Psychol.: Learn.
Mem. Cogn. 35 (3), 709.
Freeman, H.D., Beer, J.S., 2010. Frontal lobe activation mediates
the relation between sensation seeking and cortisol increases.
J. Pers. 78 (5), 14971528.
Funder, D.C., Colvin, C.R., 1988. Friends and strangers: acquaintanceship, agreement, and the accuracy of personality
judgment. J. Pers. Soc. Psychol. 55 (1), 149.
Galvan, A., Hare, T.A., Voss, H., Glover, G., Casey, B.J., 2007. Risktaking and the adolescent brain: who is at risk? Dev. Sci. 10,
F8F14.
Geniole, S.N., Carr, J.M., McCormick, C.M., 2011. State, not trait,
neuroendocrine function predicts costly reactive aggression in
men after social exclusion and inclusion. Biol. Psychol. 87 (1),
137145.
Gneezy, U., Potters, J., 1997. An experiment on risk taking and
evaluation periods. Q. J. Econ., 631645.
Goudriaan, A.E., Lapauw, B., Ruige, J., Feyen, E., Kaufman, J.M.,
Brand, M., Vingerhoets, G., 2010. The inuence of high-normal
testosterone levels on risk-taking in healthy males in a 1-week
letrozole administration study. Psychoneuroendocrinology 35
(9), 14161421.
Hao, L., Hotz, J.V., Jin, G.Z., 2008. Games parents and adolescents play: risky behaviors, parental reputation, and strategic
transfers. Econ. J. 118 (528), 515555.
Hayes, A.F., 2013. Introduction to Mediation, Moderation, and Conditional Process Analysis. The Guilford Press, New York.
Hermans, E.J., Bos, P.A., Ossewaarde, L., Ramsey, N.F., Fernndez,
G., Van Honk, J., 2010. Effects of exogenous testosterone on
the ventral striatal BOLD response during reward anticipation in
healthy women. Neuroimage 52 (1), 277283.
Hopko, D.R., Lejuez, C.W., Daughters, S.B., Aklin, W.M., Osborne,
A., Simmons, B.L., Strong, D.R., 2006. Construct validity of the
balloon analogue risk task (BART): relationship with MDMA use by
98
inner-city drug users in residential treatment. J. Psychopathol.
Behav. Assess. 28 (2), 95101.
Hoyle, R.H., Fejfar, M.C., Miller, J.D., 2000. Personality and sexual
risk taking: a quantitative review. J. Pers. 68 (6), 12031231.
Hunt, M.K., Hopko, D.R., Bare, R., Lejuez, C.W., Robinson, E.V.,
2005. Construct validity of the balloon analog risk task (BART)
associations with psychopathy and impulsivity. Assessment 12
(4), 416428.
Johnson, E.O., Kamilaris, T.C., Chrousos, G.P., Gold, P.W., 1992.
Mechanisms of stress a dynamic overview of hormonal and
behavioral homeostasis. Neurosci. Biobehav. Rev 16, 115130.
Kandasamy, N., Hardy, B., Page, L., Schaffner, M., Graggaber, J.,
Powlson, A.S., Coates, J., 2014. Cortisol shifts nancial risk preferences. Proc. Natl. Acad. Sci. 111 (9), 36083613.
Ketterson, E.D., Atwell, J.W., McGlothlin, J.W., 2009. Phenotypic
integration and independence: hormones, performance, and
response to environmental change. Integr. Comp. Biol. 49 (4),
365379.
Lauriola, M., Panno, A., Levin, I.P., Lejuez, C.W., 2014. Individual
differences in risky decision making: a meta-analysis of sensation
seeking and impulsivity with the balloon analogue risk task. J.
Behav. Decis. Mak. 27 (1), 2036.
Lejuez, C.W., Aklin, W.M., Zvolensky, M.J., Pedulla, C.M., 2003.
Evaluation of the balloon analogue risk task (BART) as a predictor
of adolescent real-world risk-taking behaviours. J. Adolesc. 26
(4), 475479.
Lejuez, C.W., Read, J.P., Kahler, C.W., Richards, J.B., Ramsey, S.E.,
Stuat, G.L., Strong, D.R., Brown, R.A., 2002. Evaluation of a
behavioral measure of risk taking: the balloon analogue risk task
(BART). J. Exp. Psychol: Appl. 8 (2), 7584.
Lewis, A.H., Porcelli, A.J., Delgado, M.R., 2014. The effects of
acute stress exposure on striatal activity during Pavlovian conditioning with monetary gains and losses. Front. Behav. Neurosci.
8, 179, http://dx.doi.org/10.3389/fnbeh.2014.00179.
Liening, S.H., Stanton, S.J., Saini, E.K., Schultheiss, O.C., 2010.
Salivary testosterone, cortisol, and progesterone: two-week stability, interhormone correlations, and effects of time of day,
menstrual cycle, and oral contraceptive use on steroid hormone
levels. Physiol. Behav. 99 (1), 816.
Lighthall, N.R., Mather, M., Gorlick, M.A., 2009. Acute stress
increases sex differences in risk seeking in the balloon analogue
risk task. PLoS ONE 4 (7), e6002.
Lin, H., Yuan, K.M., Zhou, H.Y., Bu, T., Su, H., Liu, S., Ge, R.S.,
2014. Time-course changes of steroidogenic gene expression and
steroidogenesis of rat leydig cells after acute immobilization
stress. Int. J. Mol. Sci. 15 (11), 2102821044.
Mttnen, I., Jokela, M., Hintsa, T., Firtser, S., Khnen, M.,
Jula, A., Keltikangas-Jrvinen, L., 2013. Testosterone and
temperament traits in men: longitudinal analysis. Psychoneuroendocrinology 38 (10), 22432248.
Maner, J.K., Gailliot, M.T., Menzel, A.J., Kunstman, J.W., 2012.
Dispositional anxiety blocks the psychological effects of power.
Pers. Soc. Psychol. Bull. 38 (11), 13831395.
Maner, J.K., Richey, J.A., Cromer, K., Mallott, M., Lejuez, C.W.,
Joiner, T.E., Schmidt, N.B., 2007. Dispositional anxiety and riskavoidant decision-making. Pers. Indiv. Diff. 42 (4), 665675.
Mata, R., Josef, A.K., Samanez-Larkin, G.R., Hertwig, R., 2011. Age
differences in risky choice: a meta-analysis. Ann. N. Y. Acad. Sci.
1235 (1), 1829.
Mazur, A., Booth, A., 1998. Testosterone and dominance in men.
Behav. Brain Sci. 21 (03), 353363.
Mehta, P.H., Beer, J., 2010. Neural mechanisms of the
testosteroneaggression relation: the role of orbitofrontal
cortex. J. Cogn. Neurosci. 22 (10), 23572368.
Mehta, P., Jones, A., Josephs, R., 2008. The social endocrinology
of dominance: basal testosterone predicts cortisol changes and
behavior following victory and defeat. J. Pers. Soc. Psychol. 4,
10781093.
99
van der Loos, M.J., Haring, R., Rietveld, C.A., Baumeister, S.E.,
Groenen, P.J., Hofman, A., Thurik, A.R., 2013. Serum testosterone levels in males are not associated with entrepreneurial
behavior in two independent observational studies. Physiol.
Behav. (119), 110114.
Van Honk, J., Schutter, D.J., Hermans, E.J., Putman, P., Tuiten, A.,
Koppeschaar, H., 2004. Testosterone shifts the balance between
sensitivity for punishment and reward in healthy young women.
Psychoneuroendocrinology 29 (7), 937943.
van Wingen, G., Mattern, C., Verkes, R.J., Buitelaar, J., Fernndez,
G., 2010. Testosterone reduces amygdalaorbitofrontal cortex
coupling. Psychoneuroendocrinology 35 (1), 105113.
Vazire, S., 2006. Informant reports: a cheap, fast, and easy method
for personality assessment. J. Res. Pers. 40 (5), 472481.
Vazire, S., 2010. Who knows what about a person? The self-other
knowledge asymmetry (SOKA) model. J. Pers. Soc. Psychol. 98
(2), 281.
Vazire, S., Carlson, E.N., 2011. Others sometimes know us better
than we know ourselves. Curr. Dir. Psychol. Sci. 20 (2), 104
108.
Veer, I.M., Oei, N.Y., Spinhoven, P., Van Buchem, M.A., Elzinga,
B.M., Rombouts, S.A., 2012. Endogenous cortisol is associated with functional connectivity between the amygdala and
medial prefrontal cortex. Psychoneuroendocrinology 37 (7),
10391047.
Ventura, T., Gomes, M.C., Carreira, T., 2012. Cortisol and anxiety
response to a relaxing intervention on pregnant women awaiting
amniocentesis. Psychoneuroendocrinology 37 (1), 148156.
Vermeersch, H., Tsjoen, G., Kaufman, J.M., Vincke, J., 2008. The
role of testosterone in aggressive and non-aggressive risk-taking
in adolescent boys. Horm. Behav. 53 (3), 463471.
Viau, V., 2002. Functional cross-talk between the hypothalamicpituitary-gonadal and -adrenal axes. J. Neuroendocrinology 14,
506513.
Welker, K.M., Goetz, S.M.M., Carr, J.M., 2015. Perceived and
experimentally manipulated status moderate the relationship
between facial structure and risk taking. Evol. Hum. Behav. (in
press).
Welker, K.M., Lozoya, E., Campbell, J.A., Neumann, C.S.,
Carr, J.M., 2014. Testosterone, cortisol, and psychopathic
traits in men and women. Physiol. Behav. 129, 230236,
http://dx.doi.org/10.1016/j.physbeh.2014.02.057.
White, T.L., Lejuez, C.W., de Wit, H., 2008. Test-retest characteristics of the Balloon Analogue Risk Task (BART). Exp. Clin.
Psychopharmacol. 16 (6), 565.
White, R.E., Thornhill, S., Hampson, E., 2006. Entrepreneurs and
evolutionary biology: The relationship between testosterone and
new venture creation. Organ. Behav. Hum. Decis. Process. 100
(1), 2134.
Zethraeus, N., Kocoska-Maras, L., Ellingsen, T., von Schoultz, B.,
Hirschberg, A.L., Johannesson, M., 2009. A randomized trial of
the effect of estrogen and testosterone on economic behavior.
Proc. Natl. Acad. Sci. U. S. A. 106 (16), 65356538.
Zilioli, S., Mehta, P.H., Watson, N.V., 2014a. Losing the battle but
winning the war: uncertain outcomes reverse the usual effect of
winning on testosterone. Biol. Psychol. 103, 5462.
Zilioli, S., Ponzi, D., Henry, A., Maestripieri, D., 2014b.
Testosterone, cortisol and empathy: evidence for the
dual-hormone hypothesis. Adapt. Hum. Behav. Physiol.,
http://dx.doi.org/10.1007/s40750-014-0017-x.
Zuckerman, M., 1991. Psychobiology of Personality. Cambridge University Press, New York.
Zuckerman, M., Kuhlman, D.M., 2000. Personality and risk-taking:
common biosocial factors. J. Pers. 68 (6), 9991029.